6-7 Flashcards
Motor speech disorders include
Apraxia & dysarthria
Types of apraxia of speech
Dyspraxia
Aphemia
Peripheral motor aphasia
Apraxic Dysarthria
To act or move
Praxis
A mean -
Without
Apraxia means: to not _____ per to not ___
To not act or to not move
Apraxia means lack of movement or action for speech production
Various kinds of apraxia
Inability to move eyes, limbs, and structures
An acquired disorder of speech originating from an inability to create and sequence motor plans for speech
Apraxia of speech
Apraxia of speech May co-occur with dysarthria. True or false
True
Apraxia of speech Usually co-occurs with some kind of aphasia . True or false
True
Common that a person has apraxia of speech without some language impairments. Tue or false
False. Rare that a person has apraxia of speech without some language impairments
Apraxia of speech; Rooted in an inability to ______the neural impulses necessary to create appropriate motor movements for speech
Rooted in an inability to create and sequence (program) the neural impulses necessary to create appropriate motor movements for speech
Apraxia of speech Construction of appropriate motor plans for movements of the articulators to produce non-speech actions are unaffected.
Not a single structure in the CNS, but a network of structures that all contribute to the function of putting together appropriate motor plans for speech.
Certain left hemisphere structures play a large role
For apraxia of speech
- Broca’s area and supplementary motor cortex
2.Primary motor cortex, basal ganglia, and cerebellum
Characteristics of Apraxia of Speech
Effortful speech
Aware of speech errors
Self-repairs
Struggle and frustration
Characteristics of Apraxia of Speech Cont.
Limited prosody
Slowed rate- to avoid errors
Inconsistent errors- Islands of intact speech
Visible, auditory groping of the tongue, lips, and mandible
Resonance, respiration coordination, and phonation left relatively intact
Articulation errors Usually occur on the ____ phoneme
Usually occur on the first phoneme
The more ___ the word, the more likely an error will occur
Complex
Articulation errors
Consonant clusters of /l/ and /s/
Common articulation errors in apraxia of speech
Usually occur on the first phoneme
The more complex the word, the more likely an error will occur
Consonant clusters of /l/ and /s/
Might produce different error patterns on the same word
Phoneme substitutions and distortions
Articulation errors cont.
Perseverative substitutions
Anticipatory substitutions
Phoneme additions
Phoneme prolongations
Voicing errors
Damage to the left hemisphere at or around —________
Inferior posterior frontal lobe
Etiologies of apraxia of speech
Any process or event that damages the left inferior-posterior frontal lobe
Etiologies of apraxia of speech
Any process or event that damages the left inferior-posterior frontal lobe
Usually stroke involving occlusion of the left middle cerebral artery
Generalized head trauma
Focal head trauma- surgical removal of tumor or aneurysm near Broca’s area
A neurodegenerative condition in which patients display a slow onset of apraxia of speech that gains in severity over time as a result of continued atrophy of the lateral premotor cortex and the supplementary motor area
Primary progressive apraxia of speech
Evolves into a condition of degeneration of
-The premotor cortex, prefrontal cortex, primary
-Motor cortex, basal ganglia, midbrain, and corpus callosum
Primary progressive apraxia of speech
Inability to program and carry out any volitional movements of the tongue, lips, pharynx, or larynx on command
Buccofacial Oral Apraxia
A.K.A. noverbal apraxia or oral apraxia
May be able to move articulators in a natural context, though not on command
Oral apraxia
Volitional speech can be affected, with more formulaic and automatic utterances left unimpaired
Oral apraxia
Inability to program motor movements for the use of tools and the pantomiming of gestures despite possessing the knowledge of how the object is used and its function
Ideomotor apraxia
May be able to explain the purpose and how to use a hairbrush, but cannot complete the task on command (though can complete the task in a natural context)
Ideonotor apraxia
Inability to:
Conceptualize a task
Formulate motor plans required for the task
Hold the idea of the task long enough to accomplish the task successfully
Ideational apraxia
May be able to perform individual components of a task, but cannot perform the series of actions sequentially to accomplish the entire act
Raise a hairbrush to their head, but unable to accomplish the remaining actions necessary
Cannot perform the task volitionally or automatically
Ideational apraxia
Concomitant disorders of apraxia of screech
Hemiplegia or hemiparesis
Hyperflexia
Dysarthria
Buccofacial oral apraxia/ideomotor apraxia
Nonfluent aphasia
Contralateral to the lesion
Usually affects written language by weakening dominant writing hand, while the apraxia of speech affects verbal output of language
Hemiplegia or hemiparesis
Extrapyramidal impulses of reflex regulation unable to reach the brainstem and spinal cord
Damage to the upper motor neurons with transmit extrapyramidal impulses of reflex regulation to the brain stem and spinal cord.
Hyperflexia
Articulation errors occur more often on longer/complex words
Errors are varied and inconsistent
More difficulty producing volitional than reflexive automatic utterances
Buccofacial-oral apraxia more likely
Normal muscle strength, muscle tone, and appropriate ROM
Apraxia
Articulation errors occur on all words in all utterances
Errors are consistent and predictable
Buccofacial-oral apraxia less likely
Impaired oral/ velopharyngeal muscle strength, abnormal muscle tone, and limited ROM
Dysarthria
The presence of motor speech disorders often implies a problem with the nervous system, which may validate a medical-neurological disease.
Components of evaluation
Identification of confirmatory signs to support hypothesized motor speech diagnosis
Instrumental measures
Administration of a formal test of apraxia of speech, dysarthria, and/or speech intelligibility
Examination of the patient’s individual oral structures and articulators, and observation of nonspeech functions of these structures
Eval
Tests patient’s maximum limit of ability by comparing patient’s greatest effort on a task with the known average performance rate of unimpaired individuals
Maximum performance task
Alternating motion rates (AMRs)
Simple repetitive motor tasks used to test speed and regularity
Diadochokinetic rates (DDKs)
Rapid repetition of more than one syllable at a time to test ability to rapidly move articulators successfully and precisely
Sequential motion rates (SMRs)
Types. Of maximum performance tasks
Diadochokinetic rates (DDKs)
Sequential motion rates (SMRs)
Patient produces continuous speech for at least 5 minutes.
-See if person becomes fatigued
-See how fatigue affects speech
Speech stress test
If speech degrades over 5 minutes or less due to fatigue, this is indicative of _-__
If speech degrades over 5 minutes or less due to fatigue, this is indicative of pathology
Speech tasks include
Verbal repetitions of words, phrases, and sentences
Oral reading tasks of various length
Patient’s ability to produce connected and spontaneous speech is appropriately assessed:
Asking open-ended questions
Verbally describing a picture presented
Telling or retelling of a story
No pharmaceuticals or prosthetics are used to treat Apraxia.
Three therapy treatment approaches to treat apraxia of speech:
Three therapy treatment approaches:
Articulatory kinematic therapy
Intersystemic reorganization
Alternative/augmentative communication strategies
Relies on motor learning theory and neuroplasticity to re-establish motor planning abilities for speech
Articulatory kinematic s approach
Lost motor abilities can be retrieved or rebuilt by cueing the brain to produce or access the motor plans despite brain damage
Articulatory kinematic app rich
_____ relies on three components:
1. Motor practice
2. Middling repetition
3. Articulatory cueing
Articulatory kinematic s approach
Intensive and repetitive production of target phonemes in isolation or within words or phrases to increase articulatory ability
Motor practice
Intensive and repetitive production of target phonemes in isolation or within words or phrases to increase articulatory ability
Modeling repetition
Phonetic placement descriptions given by SLP to increase patient’s awareness and understanding of articulatory movements needed to produce the target word
Articulatory queuing
Provides tactile kinesthetic, visual, and auditory cues to elicit production of target phoneme
Phonemes for Restructuring Oral Muscular Phoneme Targets (PROMPT)
PROMPT Uses touch and motion cues to the patient’s head, face, or neck at different points to illustrate:
lace of articulation
Muscles used for phoneme production
Level of tension in muscles
Voicing
Nasality
Movement of articulators
Timing/speech of movement
Degree of opening mandible
Capitalizes on a patient’s intact ability to produce melody in spite of loss of speech
Melodic intonation therapy
Pairing a physical act (gesture) not previously paired with speech with the simultaneous production of a target word
Intersystemic reorganization
Only used for long-term use with those who have severe or profound levels of apraxia of speech
Augmentative and alternative strategies
Group of disorders produced by damage to the CNS or PNS, which results in disordered movement that affects speech production
Dysarthria
Each dysarthria has its own specific profile of speech and physiological characteristics that are the result of the site of damage in the CNS or PNS
Dysarthria types
Flaccid
Spastic
Unilateral upper motor neuron
Ataxic
Hypokinetic
Hyperkinetic
*Mixed
On one side q
Unilateral
On both sides
Bilateral
On the same side q
Ipsilateral
On the opposite side
Contralateral
Partial or incomplete loss of movement (weakness)
Paresis
Total loss of movement
Paralysis
Abnormal change in body tissue, usually as a result of disease or trauma
Lesion
Systems supporting the production of speech, which includes articulatory, phonatory, and respiratory systems
Speech systems
lack of appropriate muscle tone
Hypotonic
excess/tightness of muscle tone
Hypertonic
L ack of appropriate reflexes
Hypo reflex ia
excess/overactive reflexes
Hyper reflex ia
Lack of appropriate level of movement
Hypokinetic
excess or too much movement to be appropriate
Hyperkinetic
Results from flaccid weakness or paralysis of musculature used to produce speech
Created by low muscle tone (hypotonia) and weakness in the muscle
FLACCID dysarthria
Ethnologies of flaccid dysarthria
Created by damage to the LMNs of the cranial nerves or to connections between LMNs and muscle fibers
Infections
Autoimmune/neurodegenerative diseases
Surgical trauma
Tumor
Toxins
Mass effect
Congenital syndromes
Brainstem stroke to cranial nuclei
Damage to lower motor neurons (LMNs) of the cranial nerves
Typically seen in
Flaccid dysarthria
Damage to LMNs of cranial nerves is usually where they synapse at the brainstem at the cranial nerve nuclei
Flaccid dysarthria
Trigeminal nerve damage has three branches:
Has three branches
Ophthalmic: sensory branch
Maxillary: sensory branch
Mandibular: motor to mandible
Lesion to right or left nerve will weaken/disable corresponding side of the mandible
Unilateral trigeminal nerve damage
Contralateral and undamaged side of the mandible still functional
Unilateral trigeminal nerve damage
Mandible will deviate toward side of damage
Unilateral trigeminal nerve damageq
Both right and left nerve damage weakens or paralyzes the right and left side of mandible
Bilateral trigeminal nerve damage
May be unable to raise mandible for articulation or mastication purposes
Bilateral traigmental nerve damage
Facial never damage divided in 4 branches
Divided into four branches:
Temporal: innervates muscles around eyes and movement of forehead for facial expression
Buccal: innervate muscles of the lower face to control lips and compression of cheeks
Zygomatic: innervate muscles of the lower face to control lips and compression of cheeks
Mandibular: innervate muscles of the lower face to control lips and compression of cheeks
Inability to move muscles of the face from lesion that occurs before division of nerve
Unilateral facial nerve damage
Unilateral lesion will decrease motor function ipsilaterally
Unilateral facial nerve damage
Facial asymmetry will be present
:
Facial asymmetry will be present
Weakened side of the lips will sag below unaffected side of the lips
Air will leak from affected side of the lips when inflating cheeks
Difficulty blinking affected eye and/or ptosis (droopy eyelid) may occur on affected side
On the affected side of the face, the eyebrow will have decreased range of motion and forehead will be smooth and unwrinkled
Articulation of phonemes requiring strong labial seal may be mildly impaired
Unilateral facial nerve damage
Bilateral facial weakness
May be unable to bring lips together at all
Cannot produce bilabial or labiodental phonemes
Bilateral facial nerve damage
Courses through head and neck before moving into thorax
Branches of vagus innervate many important structures for speech
Vargas nerve damage
Innervates muscles of pharynx and velum
Weakness on ipsilateral side of pharynx and velum with contralateral function intact
Unilateral Vargas nerve to the pharyngeal plexus
Damage to right and left pharyngeal plexuses
Bilateral vagus nerve damage to the pharyngeal plecxus
Passes under subclavian artery on the right and under the aorta on the left to course back up superioriorly to innervate all intrinsic muscles of the larynx (except cricothyroid)
Unilateral recurrent laryngeal nerve damage
Vocal folds paralyzed at midline
Unable to approximate for phonation
Respiration may be difficult
Bilateral recurrent laryngeal nerve damage
Innervates intrinsic and extrinsic muscles of the tongue (except palatoglossus)
Unilateral damage causes weakness on side of tongue ipsilateral to lesion
Unilateral hypoglossal nerve damage
Bilateral lingual weakness
Difficulty protruding the tongue
Reduced lingual range of motion
Confirmatory signs of Flaccid Dysarthria
Lower motor neuron damage may result in
Hypotonia
Muscle atrophy
Fasciculations
Hyporeflexia
Created by spasticity in muscles associated with speech production
Spastic dyarthria
Upper motor neurons (UMNs) are descending (efferent) tracts of axons that begin in cerebral cortex and travel within the CNS to synapse with LMNs of PNS
Spastic dysarthria
Origin of spastic dysarthria is bilateral damage to UMNs
Q
Confirmatory signs of Spastic Dysarthria
Bilateral UMN damage creates:
Hypertonia
Hyperreflexia
Lesion bilaterally to the UMNs will create effects seen on both sides of the body
Spastic dysarthria
Incoordination
Produces a slushy or drunken-like speech quality
Imprecise production of consonants, excess and equal stress, and irregular articulatory breakdowns
Weakness will not be present
All oral and facial structures will appear normal at rest
Signs appear only during movement
Ataxic dysarthria q
Result of pathology of the cerebellum
Responsible for monitoring and correcting errors in timing, range, force, and direction of motor movements in the motor plan
Ataxic dysphasia q
Confirmatory signs of Ataxic Dysarthria
Not confined to speech production alone
May display signs of decreased cerebellar functioning in addition to ataxic dysarthria
Ataxic gait
Dysmetria
Over- or undershooting the of the movement of a body part while performing a volitional movement
Dysmetria q
Feet usually spread broadly apart, with irregular foot steps and a greater likelihood of falls
Ataxic gait q
Result of pathology at the basal ganglia or its connections to other structures in CNS
Neuromotor basis is rigidity, reduced amounts of volitional movement, and reduced range of motion in the movement remaining
Hyperkinetic dysarthria
Movements of structures of speech systems become erased entirely or reduced in range of motion
Hpokinetic dysarthria q
Damage to structures of the basal ganglia or the connections between the structures of the basal ganglia and other CNS structures
Hypokinetic dysarthriaq
Damage creates rigid muscle tone, postural abnormalities, difficulties initiating movement, deficits in ability to learn new motor movements, and tremors at rest
Hypokinetic dysartihea q
